White lesions Flashcards

1
Q

Explain why the normal mucosa appears pink

A
  • Light shines through the epithelium into the underlying connective tissues
  • Light reflects from the haemoglobin in erythrocytes found in the vasculature of the connective tissues
  • That light is bounced back to the eye of the observer and we see “pink”.
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2
Q

Explain why white lesions appear white

A

A blockage of light which is normally reflected from the haemoglobin in erythrocytes in the blood vessels of the connective tissue to the observer’s eyes

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3
Q

List 6 examples of white lesions

A
  • Hyperkeratosis
  • Parakeratosis
  • Acanthosis
  • Spongiosis (Intracellular Oedema)
  • Ulceration and Inflammation
  • Superficial Fungal Infection
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4
Q

Explain what hyperkeratosis is

A
  • Hyper(ortho)keratosis is the excess formation of mature keratin
  • It is likely the most common reason for a lesion to appear white
  • The thick layer of material covering the epithelium is orthokeratin.
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5
Q

Explain what parakeratosis is

A
  • Parakeratosis is immature keratin formation. Immature keratin has nuclei in it, unlike orthokeratin
  • Often, orthokeratin and parakeratin are present together in the same lesion
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6
Q

Define acanthosis

A
  • Acanthosis is thickening of the epithelium due to increased number of cells. (Hyperplasia)
  • This has the effect of placing an avascular band of tissue between the observer and the underlying blood vessels.
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7
Q

Define spongiosis

A
  • Spongiosis (or intracellular oedema)

* The epithelium may collect fluid or become oedematous.

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8
Q

Explain why inflammation can appear as white

A
  • Chronic inflammation in the connective tissue has a tendency to block the red reflection
  • This has the effect of thickening the area between the surface and the underlying blood vessels.
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9
Q

Explain why ulceration appears as white

A

Ulcerated areas may have a yellowish white appearance due to the deposition of a thick layer of coagulated exudate on the surface.

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10
Q

Explain superficial fungal debris

A
  • White lesion on the oral mucosal surface reflecting fungal colonies (e.g. candida) infecting the surface epithelium
  • Often presents with inflammation and epithelial hyperplasia (acanthosis).
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11
Q

Explain what to do when you see a patient with a lesion

A
  • I/O and E/O
  • Medical history, social history
  • Onset, severity, frequency, pain, signs/ symptoms
  • Location, distribution, size, shape/margins, colour, consistency, tactility (e.g. Induration, Fixation), pain on palpation, interaction with neighbouring structures
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12
Q

List the possible categories that a lesion could fall

A
  • Developmental/Hereditary
  • Traumatic (Physical, Chemical, Thermal, Radiation)
  • Infective (Bacterial, Viral, Fungal)
  • Immune Mediated
  • Metabolic
  • Nutritional
  • Neoplastic
  • Iatrogenic (Procedural/Treatment)
  • Idiopathic (No Known Cause)
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13
Q

Explain what Fordyce granules are

A
  • Fordyce’s Granules are benign sebaceous glands. They are a variation of normal oral phenotype
  • Asymptomatic, yellow-white 1-3mm macule and papules typically seen on buccal mucosa and upper lip vermillion
  • Generally bilateral and symmetrically distributed.
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14
Q

Explain what white sponge nevus is in terms of genetics and appearance

A
  • Rare autosomal dominant disorder which affects the oral and other mucosae; but not the skin
  • Asymptomatic, thick, white spongy plaques usually on buccal mucosa, ventral tongue, lip mucosa and soft palate
  • Mutation in genes associated with keratin-4 (KRT4) or keratin-13 (KRT13); resulting in keratin instability and aggregation of tonofilaments
  • This is a benign inherited condition –there is no treatment.
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15
Q

Explain what leukodema is

A
  • Leukoedemais a variation of normal.
  • Caused by mild local irritation – e.g. smoking, toothpastes, mouthrinses, physical trauma
  • Asymptomatic, white-grey translucent linear reticulations, commonly on buccal mucosa, and less frequently on lip mucosa or ventral tongue
  • There is complete disappearance of these reticulations upon stretching the mucosa (the “stretch test”) is a diagnostic feature.
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16
Q

Explain what morsicatio mucosae oris

A
  • A benign, chronic trauma-induced lesion of the oral mucosa
  • Asymptomatic, poorly demarcated, thickened, white, ragged, papules and plaques
  • The most common sites are the buccal mucosae (Morsicatio Buccarum), lateral/ventral tongue (Morsicatio Linguarum) and lower lip mucosa (Morsicatio Labiorum)
  • Para-functional Habit?
17
Q

Explain what nicotinic stomatitis is and how it occurs

A
  • An inflammatory condition of the hard palate mucosa; commonly seen with pipe, cigar or reverse smokers
  • As a result of chronic exposure to heat, the palatal mucosa becomes hyperkeratotic and thickened, and the surface often contains scattered 1-3mm red punctuate papules which are the inflamed orifices of minor salivary gland ducts
18
Q

Explain what hairy tongue is

A
  • Hairy Tongueis a benign elongation of filiform papillae and retention of keratin resulting in hair-like appearance on the dorsum of the tongue
  • Can be stained by food, tobacco or chromogenic bacteria
  • Dry Mouth – lack of saliva to clear keratin
  • Poor Diet – reduced mechanical desquamation of keratin if consuming soft, processed foods.
19
Q

Explain benign migratory glossitis

A
  • A chronic benign inflammatory condition involving relapsing-recurring loss of filiform papillae. Can be sensitive to spicy or acidic food.
  • Unknown aetiology. Often occurs in patients with a history of eczema, allergies, or psoriasis
  • Lesions tend to flare when patients are under stress or ill
  • Self-limiting, heals within a few days; but does recur.
20
Q

Explain what candidiasis is

A
  • Occurs as an opportunistic infection. Can be a strong predictor of AIDS progression
  • Pseudomembranous candidiasis: white, curdy papules and plaques composed of tangled hyphae, yeast, and desquamated epithelial cells
  • Hyperplastic candidiasis: asymptomatic white plaques that cannot be scraped off.
21
Q

Explain oral hairy leukoplakia

A
  • A benign condition of the tongue caused by Epstein-Barr virus (EBV)
  • It is most frequently seen in immunocompromised patients such as those with HIV/AIDS as well as in patients on immunosuppressive therapy such as organ transplant recipients.
  • Presents most frequently on the lateral borders of the tongue as an asymptomatic, white, adherent plaque with linear folds that run parallel to the long axis of the tongue.
22
Q

Explain what oral lichen planus is as well as its sub classifications

A
  • Immune-mediated condition in which basal cells are destroyed by cytotoxic CD8+ T cells
  • Typical oral LP is almost always bilateral and symmetric and affects the buccal mucosa, tongue, and attached gingiva.

Lesions may be classified into the following, often overlapping categories:
• Reticular - white intersecting loops and lines forming Wickham striae or papules
• Erosive– i.e. desquamative gingivitis
• Ulcerative– yellow fibrin membrane with an erythematous rim and subtle reticulations
• Atrophic– loss of papillae and diffuse keratosis or white papules
• Bullous– presenting with bullae which break down to form erosive OLP

23
Q

Explain what lichenoid reactions are, how it is caused and how it appears histologically

A
  • These lesions are collectively termed Lichenoid Reactions and encompass lichenoid drug reactions and lichenoid reactions to dental materials
  • Anti-hypertensives, diuretics, NSAIDs, anti-convulsants, anti-malarials, chemotherapy agents, amalgam, gold can cause them
  • May range from asymptomatic striae and plaque-like lesions to painful erythematous and ulcerative lesions.
  • Histopathologically OLR appear similar to OLP -showing a band-like infiltrate (mainly T cell) within the lamina propria as well as degeneration of the basal cell layer.
24
Q

Explain what actinic cheilitis is

A
  • Actinic Chelitisis most commonly due to chronic sun exposure and is typically seen on the lower lip of adults with fair skin who have significant sun exposure and may be as common as 9–40%
  • UV (ultraviolet) radiation-induced DNA damage leads to morphological changes of keratinocytes
  • The affected lip is often dry, scaly, fragile, cracked, with thickened plaques and papules
  • There may also be white or yellow areas, with crusting, erosions, or focal ulceration
25
Q

Define leukoplakia

A
  • Leukoplakia is defined as a “white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer”
  • Approximately 40% of leukoplakia show features of dysplasia, carcinoma-in-situ or invasive squamous cell carcinoma
  • The other 60% will show hyperkeratosis or parakeratosis, acanthosis, or atrophy, with or without inflammation; these have been given the name keratosis of unknown significance
  • The greater the degree of dysplasia; the greater the risk of malignant transformation.
26
Q

List some important clinical steps to take when you see a lesion in a patient

A
  • All lesions should be palpated to evaluate for firmness or induration(and fixation), which may indicate the presence of an invasive carcinoma
  • The sites with the highest incidence of development of squamous cell carcinoma are the ventral tongue, floor of mouth, buccal mucosa, and gingiva
  • Although the soft palate is an uncommon site for leukoplakia, it has a high prevalence of dysplasia or carcinoma when it does occur.